Initial traumatic brain injury (TBI) may cause immediate damage to cerebral structure, neurons, or vasculature. Secondary injuries that follow TBI may include ischemia, swelling, cerebral edema, and increased intracranial pressure. In general, these secondary complications may lead to reduction in the supply of oxygenated blood to the brain (brain ischemia) which may lead to neurodegeneration. In addition to TBI, brain ischemia may be caused by stroke, cardiac arrest, and respiratory failure, the three leading causes of death in the United States.
The secondary injury mechanism following a traumatic event generally results in cell death from lack of blood and will typically begin after about 30 minutes of disrupted blood supply. Prolonged oxygen deprivation may cause failure of autoregulation and programmed cell death. Thus, it is important that intervention is performed within the first 6 hours after the initial injury.
Evidence suggests that selectively cooling the brain temperature to about 32-35° C. (therapeutic hypothermia), (See e.g., Andrews et al., European Society of Intensive Care Medicine Study of Therapeutic Hypothermia (32-35 C) for Intracranial Pressure Reduction After Traumatic Brain Injury (The Eurotherm3235Trial). Trials 12(1): 8, (2011), incorporated by reference herein) or maintaining brain temperature in the normal range (target temperature management) early in the therapeutic window, e.g., less than about 30 minutes after injury, may delay necrotic cell death and apoptotic cell death. This may lead to positive effects including, inter alia, a lower cerebral metabolism which reduces harmful metabolic byproduct build up resulting from inadequate blood flow, reduced cerebral oxygen requirements, prevention of neurogenic fever, reduced intracranial pressure (ICP) encephalitis, and the like.
There are currently Class 1 and Class 2 recommendations for therapeutic hypothermia (TH) and target temperature management (TTM) after certain ischemic brain injuries. Target temperature management and therapeutic hypothermia has been indicated for several ischemic injuries and evidence. See. e.g., Abou-Chebl et al., Local Brain Temperature Reduction Through Intranasal Cooling With the RhinoChill Device, Stroke 42(8): 2164-2169, (2011), Takeda et al., Effects of Pharyngeal Cooling on Brain Temperature in Primates and Humans A Study for Proof of Principle, The Journal of the American Society of Anesthesiologists, 117(1): 117-125.2012, (2012), and Springborg et al., First Clinical Experience With Intranasal Cooling for Hyperthermia in Brain-injured Patients, Neurocritical care, 18(3): 400-405, (2013), all incorporated by reference herein. All Class I Level of Evidence (LOE) B—Class III LOE C points towards increased favorable outcomes, reduced length of ICU stay, and improved neurological function at about 6 months after injury.
One conventional system for cooling tissue is disclosed in U.S. Publ. No. 2013/0000642 to Fearnot et al., incorporated by reference herein. Disclosed in the '642 patent application is a system which relies on forced air that is not cooled. Even if the '642 patent application is capable of cooling the forced are, the mask apparatus as taught by the '642 patent application may not provide sufficient cooling to cool the brain of a human subject. Additionally, the '642 patent application fails to teach any feedback to provide any type of control over a cooling process.
Another conventional method and device for non-invasive cerebral systemic cooling is disclosed in U.S. Pub. No. 2006/0276552, incorporated by reference herein. The '655 patent application teaches a complicated and cumbersome cooling device and method which relies inserting an elongated member into a nasal cavity of a patient, injecting a perfluorocarbon spray and a gas into the nasal cavity, and using the gas to enhance evaporation of the perfluorocarbon to reduce the temperature of the brain or infusing a cooled liquid through a complicated three-part cooling assembly with a balloon and two elongated tubes placed inside the nose.
Studies on the effectiveness of brain temperature management after traumatic brain injury is extremely limited. Due to the technological limitation of conventional systems and methods, the evidence in support of conventional systems and methods to address TTM and TH exhibit at least the following drawbacks: studies examine whole body cooling rather than selective cooling of the brain which may have adverse side effects such as shivering, cooling may not be initiated within 30 minutes of injury, and consistent cooling and rewarming protocols are not followed.
Thus, there is a need for a less complex and less cumbersome system and method for cooling the brain that provides a flow of air or breathable gas that cools the brain to effectively provide TH and TTM at the point of injury or prior to hospitalization and early in the therapeutic window, monitors the temperature of the brain and human subject, and adjusts temperature and flow rate of the flow of air or breathable gas to reduce possible adverse side effects which may be associated with cooling the brain of a human subject.